The effect of green tea on oxidative damage and tumour formation in Lobund-Wistar rats.
A number of epidemiological studies suggest that the consumption of green tea reduces the incidence of prostate cancer. As the major catechins present in green tea are potent antioxidants, we hypothesized that genetic and cellular damage induced by oxygen free radicals could be significantly reduced by potent antioxidants in green tea, thus reducing the cumulative genetic and cellular damage with age, and slowing or preventing tumour formation. Long-term administration of a decaffeinated green tea extract to Lobund-Wistar rats for periods up to 26 months almost halved the incidence of primary tumours in the genitourinary tract when compared with an age-matched cohort receiving just water. We observed no inhibition of DNA adduct formation or lipid peroxidation in animals consuming green tea compared with animals consuming deionized water. The decrease in tumour formation was associated with an increase in 8-hydroxy-2'deoxyguanosine and 4-hydroxynonenal content (markers of DNA adduct formation and lipid peroxidation, respectively) in the epithelium of the ventral prostate in aging animals. In addition, there was an increase in 8-hydroxy-2'deoxyguanosine expression, but no change in 4-hydroxynonenal expression in the seminal vesicles of older animals. An age-associated increase in expression of the antioxidant enzymes manganese superoxide dismutase and catalase in the epithelium of the ventral prostate of aging animals was observed. Furthermore, there was also an increase in manganese superoxide dismutase expression, but no change in catalase expression in the seminal vesicles of older animals. These data demonstrate that consumption of green tea decreases the incidence of genitourinary tract tumours in the Lobund-Wistar rat, but has no effect on age-associated DNA adduct formation and lipid peroxidation in the ventral prostate and seminal vesicles of the aging rat.
O'Sullivan
Jacintha
J
Centre for Colorectal Disease, Education and Research Centre, St Vincents University Hospital, Dublin, Ireland.
Sheridan
Juliette
J
Mulcahy
Hugh
H
Tenniswood
Martin
M
Morrissey
Colm
C
D000080242:8-Hydroxy-2'-Deoxyguanosine; D000447:Aldehydes / Q000378:metabolism; D000818:Animals; D002374:Catalase / Q000378:metabolism; D004249:DNA Damage / Q000187:drug effects*; D003849:Deoxyguanosine / Q000031:analogs & derivatives / Q000378:metabolism; D015994:Incidence; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D009369:Neoplasms / Q000453:epidemiology / Q000378:metabolism* / Q000473:pathology*; D018384:Oxidative Stress / Q000187:drug effects* / Q000235:genetics; D010936:Plant Extracts / Q000494:pharmacology*; D011467:Prostate / Q000187:drug effects / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012669:Seminal Vesicles / Q000187:drug effects / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism; D013662:Tea / Q000737:chemistry; D014565:Urogenital Neoplasms / Q000453:epidemiology / Q000378:metabolism / Q000473:pathology
D000447:Aldehydes; D010936:Plant Extracts; D013662:Tea; D000080242:8-Hydroxy-2'-Deoxyguanosine; D002374:Catalase; D013482:Superoxide Dismutase; D003849:Deoxyguanosine; C027576:4-hydroxy-2-nonenal